Abstract

OBJECTIVE—We investigated the impact of active smoking and exposure to passive smoke on the risk of developing diabetes.

RESEARCH DESIGN AND METHODS—Data were analyzed from a cohort of participants in the High-Risk and Population Strategy for Occupational Health Promotion
Study (HIPOP-OHP) conducted in Japan from 1999 to 2004. Active and passive smoking status in the workplace was evaluated at
baseline.

RESULTS—Of 6,498 participants (20.9% women), a total of 229 diabetes cases were reported over a median 3.4 years of follow-up. In
the workplace, compared with zero-exposure subjects, the multivariable-adjusted hazard ratios of developing diabetes were
1.81 (95% CI 1.06–3.08, P = 0.028) for present passive subjects and 1.99 (1.29–3.04, P = 0.002) for present active smokers.

CONCLUSIONS—In this cohort, exposure to passive smoke in the workplace was associated with an increased risk of diabetes after adjustment
for a large number of possible confounders.

A positive association between active smoking and the incidence of diabetes has been identified (1–3). Only one study has shown a significant association between passive smoke and impaired glucose tolerance (4), and the association between exposure to passive smoke and the risk of developing diabetes has not been fully investigated.
Here, we examine the relationship between exposure to passive smoke in the workplace or at home and the risk of developing
diabetes in a large sample from a nonrandomized health promotion intervention study conducted at workplaces in Japan.

RESEARCH DESIGN AND METHODS

Analyses were performed using baseline and annual follow-up data from the High-Risk and Population Strategy for Occupational
Health Promotion Study (HIPOP-OHP) conducted between 1999 and 2004 at 12 large-scale companies, excluding prevalent diabetes
cases or those who did not report active or passive smoking status at baseline. Full-time employees at the worksites were
enrolled, and then the worksites were nonrandomly assigned to either the intervention or control groups (13–20). All participants
underwent an annual health check including blood testing at baseline and thereafter. A history of diabetes as well as lifestyle
variables such as daily alcohol intake and smoking habits were evaluated using a self-administered questionnaire (5–7).

We constructed the following four categories by combining active smoking status and passive smoking status at workplace or
at home as follows: 1) “zero exposure” included those who never smoked and were not currently exposed to passive smoke; 2) “past active only” included those who had smoked in the past but did not currently smoke and were not currently exposed
to passive smoke; 3) “present passive” included those currently exposed to passive smoke but who did not actively smoke, irrespective of past
smoking; and 4) “present active” included those who currently smoke irrespective of exposure to passive smoke.

A subject was considered diabetic if at least one of the following parameters was met: fasting blood glucose level ≥126 mg/dl
(≥7.0 mmol/l), random plasma glucose level ≤200 mg/dl (≥11.1 mmol/l), or treatment with hypoglycemic medication (insulin or
oral hypoglycemic agent). A self-reported history of diabetes was also accepted, since self-reported diagnosis of diabetes
has been shown to be reliable (8) and has been used in many cohort studies (9,10).

Statistical analyses

We used the Cox proportional hazards model to analyze the association between passive smoking and incident diabetes cases.
Person-time was calculated from the return of the baseline questionnaire until the date of the annual health check, at which
the diagnosis of diabetes was confirmed, or the end of the follow-up, whichever occurred first.

We evaluated the effect of active smoking and exposure to passive smoke on the risk of developing diabetes in a multivariable-adjusted
model, adjusting for all variables listed in Table 1. Likelihood ratio tests were used to test statistical interactions between passive smoking status and sex, BMI, or assigned
intervention.

RESULTS

Of the 6,498 participants (20.9% women), 44.6% were current smokers (average of 19.6 cigarettes smoked per day), while 12.6%
reported exposure to passive smoke in the workplace. Approximately 32% of participants dropped out during the follow-up.

CONCLUSIONS—

In this 4-year prospective study conducted in the workplace, self-reported exposure to environmental tobacco smoke in the
workplace and current active smoking at baseline were positively associated with an increased risk of developing diabetes,
even after adjustment for a large number of possible confounders. To our knowledge, only one study has explored the association
between exposure to passive smoke and subsequent risk of diabetes, which yielded similar results to our study, although not
statistically significant (4). A possible limitation of our study is that the results might be underestimated by time-dependent confounding by smoking
status; in fact, exposure to passive smoke in the workplace was not associated with the risk of diabetes in the intervention
group, possibly due to lowered exposure to passive smoke by intervention. These findings add new evidence to support the need
for measures to lessen environmental tobacco smoke in the workplace, especially in Asian populations, in which both the genetic
susceptibility to diabetes (11,12) and smoking rate (13) are generally high.

Acknowledgments

The HIPOP-OHP study was funded by research grants from the Ministry of Health and Welfare, Japan (H10-12, no. 063, Research
on Health Services, Health Sciences Research Grant; and H13, no. 010, Medical Frontier Strategy Research, Health Sciences
Research Grant), the Ministry of Health, Labor and Welfare, Japan (H14-16, no. 010, Clinical Research for Evidenced-Based
Medicine, Health and Labor Sciences Research Grant), and the Japan Arteriosclerosis Prevention Fund 2000 and 2004.

We thank Toshimi Yoshida, Department of Health Sciences, Shiga University of Medical Science, for excellent clerical support
in this research.

Footnotes

↵* A complete list of the members of the HIPOP-OHP Research Group can be found in the appendix.

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